Platelets are small (2-4 μm) discoid cells released by megakaryocytes present in the bone marrow. During this process, megakaryocytes transfer components to daughter platelets, including messenger RNA and microRNA as well as cytoplasmic organelles. Mitochondria are among these organelles and although they can amplify platelet activation and thrombosis, very little is known regarding their number and distribution in platelets.
Platelets circulate in blood to promote haemostasis and play pivotal roles in the prevention of bleeding. Structurally, platelets are small anucleated cells that contain a number of organelles including granules (a, dense and lysosomes), peroxisomes and mitochondria. While recognition of endothelial damage by platelets triggers fusion of the granules with the plasma membrane and the release of their contents, the repercussions of platelet activation on mitochondria distribution remains unknown.
Even though platelet activation is necessary to prevent or limit bleeding in a homeostatic state, their activation in other circumstances should be limited to avoid deleterious or pathological consequences. For example, to limit platelet activation, they are stored, prior to transfusion, at 22° C., which limits their shelf-life.
It would be highly desirable to be provided with methods and processes for limiting or even inhibiting platelet activation. It would also be desirable to be provided with methods and processes for detecting when modulation in platelet activity occurs (such as for example, platelet activation, platelet death and/or platelet apoptosis, sometimes referred to as “storage lesion”) or for quantifying the extent of such platelet activation. Preferably, these methods and processes would not only be applied towards platelet activation, but could also be used in determining the presence of sterile and infectious inflammatory conditions or reactions.